Bana minnu sababu ye balodɛsɛ ye olu dɔnniya ye mun ye?
Bana min bɛ wele ko alzheimers bana (AD) farati ka bon kosɛbɛ wa a bɛ sɔrɔ poroteyini dunbaliya fɛ, sumaya, ani nɔrɔli baarabaliya fɛ.
A taamasiɲɛ jɔnjɔn fila ye amiloyidi-beta (Aβ) pilakiw ni jolisiraw ɲagamini (NFTs) bɛ min na.
Amiloyidi-beta nɔnabila bɛ kɛ ni amiloyidi ɲɛci poroteyini (APP) kunkurunw farala ɲɔgɔn kan ni asidi ye ka kɛ Aβ peptide ye.
Nin peptide nunu bɛ fara ɲɔgɔn kan ka fibililɛri jii sigi min nuw bi fara ɲɔgɔn kan sɛriwɛriw kɔno, ka sɛriwɛriw ka kunnafolifalen ɲagami ɲɔgɔn na ani ka sɛriwɛriw faga.
Aβ bilala sɛnsɛnni bɛ jatɛ ina fɔ bana kɔrɔw dɔ AD yiriwali la, ani a jatɛra ka kɛ sababu ye ka fanga dɔgɔya hakili ciiw la.
Neurofibrillary tangles koun bé formé wati min tau protéine koun hyperphosphorylated ani ka filament anormal formé neuron kônon.
Nin manabɛlɛw bɛ fiɲɛ don mikɔrɔtubuliw ka baara kɛ cogo la, minnu nafa ka bon farikolojɔli ni fɛn wɛrɛw tali la ni nɔgɔw donni ye u kɔnɔ.
O kɔsɔn, o kurukuruw bɛ laban ka se ka bana in lase mɔgɔ farikolo ma.
Kɔnɔboli fana sen bɛ banafurakɛlaw ka baara la.
Farikolo tangacogo farikolo ma bɛ jabi kɛ Aβ nɔfɛlolow ni NFTs farali kan ni farilajidɛsɛ min bɛ sɔrɔ farikolo kɛrɛfɛ bolow ka se ka bana bila mɔgɔ la, min bɛ se ka fiɲɛ bila seliliw la.
Ka fara o kan, seereyaw bɛ yen ko degun bɛ farikolo degun, mitochondrial ka baarabaliya, ani guloze ka baarabaliya bɛ bana bila mɔgɔ la.
Nin sababu ninnu bɛ se ka na ni nɔrɔniw ka baara tiɲɛni ye ani ka u faga, ka dɔ fara bana juguya kan.
A ka ca a la, bana min bɛ wele ko Alzheimer bana, o sababu ye fɛn caman ye ɲɔgɔn kan minnu bɛ laban ka kɛ sababu ye ka dɔ bɔ mɔgɔ ka dɔnniya la ani ka mɔgɔw hakili bɔ.
Nemeroff CB: The preeminent role of neuropeptide systems in the early pathophysiology of Alzheimer disease: up with corticotropin-releasing factor, down with acetylcholine. Arch Gen Psychiatry. 1999, 56 (11): 991-2.
Proft J, Weiss N: Jekyll and Hide: The two faces of amyloid β. Commun Integr Biol. 2012, 5 (5): 405-7.
Whitehouse PJ, Hedreen JC, White CL, Price DL: Basal forebrain neurons in the dementia of Parkinson disease. Ann Neurol. 1983, 13 (3): 243-8.
Casadesus G, Moreira PI, Nunomura A, Siedlak SL, Bligh-Glover W, Balraj E, Petot G, Smith MA, Perry G: Indices of metabolic dysfunction and oxidative stress. Neurochem Res. , 32 (4-5): 717-22.
Candore G, Bulati M, Caruso C, Castiglia L, Colonna-Romano G, Di Bona D, Duro G, Lio D, Matranga D, Pellicanò M, Rizzo C, Scapagnini G, Vasto S: Inflammation, cytokines, immune response, apolipoprotein E, cholesterol, and oxidative stress in Alzheimer disease: therapeutic implications. Rejuvenation Res. , 13 (2-3): 301-13.
Schindler SE, McConathy J, Ances BM, Diamond MI: Advances in diagnostic testing for Alzheimer disease. Mo Med. , 110 (5): 401-5.
Singh VK: Immune-activation model in Alzheimer disease. Mol Chem Neuropathol. , 28 (1-3): 105-11.
['Kunnafoni nafama: kɛnɛya']
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['Ni i dara a la kô i ka site web ni a baara tchogow bè i ka lakananifènw la, i (walima i ka lasigiden) bè se ka i yèrè ka lakananifènw bila ka o site web ni a baara tchogow bila kènèkan.']
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["DMCA bɛ a ɲini i ka kunnafoni sɛbɛn bɔlɔlɔw kan kojugukɛ sɛbɛn bɛ sɛbɛn min kɔnɔ, o ka kan ka nin kunnafoniw fara a kan: (1) sɛbɛnni kɛtɔ ka sɛbɛnni kɛ min bɛ sɛbɛnni kɛ ni a ma kɛ kojugukɛ sɛbɛn ye; (2) sɛbɛnni kɛtɔ ka fɛn kofɔlen in kofɔ ani kunnafoni minnu bɛ a to an bɛ se ka fɛn kofɔlen in sɔrɔ; (3) i ka ladɛrɛsi, i ka ladɛrɛsi, telefɔni nimɔrɔ ani i ka ladɛrɛsi; (4) i ka kumaɲɔgɔnya sɛbɛn ko i dalen b'a la ko i bɛ a dɔn ko i bɛ ka fɛn kofɔlen in kɛ ni sariya min ye, o ma di sɛbɛnnikɛbaga ma, a ka ladɛrɛsi tigi, walima sariya wɛrɛ; "]
['(5) a ka seereyasɛbɛ sɛbɛntiya, ko seereyasɛbɛ minɛnen bɛ kojugubakɛlaw kama, ko kunnafoni min bɛ o sɛbɛntiya kɔnɔ, ko tiɲɛ don ani ko i yamaruyalen don ka yamaruya di ka kɛwalew kɛ minnu bɛ tiɲɛni kɛ; ']
['ani (6) sɛbɛn dɔ ka boloci walima ɛkitɔrɔniki sɛbɛn sɛbɛn tigi fɛ walima mɔgɔ min yamaruyara ka baara kɛ sɛbɛn tigi tɔgɔla. ']
['Ni kunnafoni fɔlen ninnu bɛɛ ma fara ɲɔgɔn kan, o bɛ se ka kɛ sababu ye ka mɛn baara kɛli la i ka sɛbɛn kɔnɔ.']
['Ɲɔgɔnkunbɛn']
['Sɛbɛn ɲɛ Ɲiningaliw / ladiliw']
What is pathophysiology of alzheimer?
The pathophysiology of Alzheimer's disease (AD) is a complex process that involves the accumulation of abnormal proteins, inflammation, and neuronal dysfunction.
The two main hallmarks of AD are the presence of amyloid-beta (Aβ) plaques and neurofibrillary tangles (NFTs) in the brain.
Amyloid-beta plaques are formed when fragments of the amyloid precursor protein (APP) are cleaved by enzymes to form Aβ peptides.
These peptides aggregate and form insoluble fibrils that accumulate outside neurons, disrupting cell-to-cell communication and leading to neuronal death.
The accumulation of Aβ plaques is thought to be one of the earliest events in the development of AD, and it is believed to contribute to the neurodegenerative process.
Neurofibrillary tangles are formed when the protein tau becomes hyperphosphorylated and forms abnormal filaments inside neurons.
These tangles disrupt the normal functioning of the microtubules, which are essential for the transport of nutrients and other materials within the neuron.
The tangles eventually lead to the death of the affected neurons.
Inflammation also plays a role in the pathophysiology of AD.
The immune system responds to the accumulation of Aβ plaques and NFTs by releasing pro-inflammatory cytokines, which can exacerbate the damage to neurons.
Additionally, there is evidence that oxidative stress, mitochondrial dysfunction, and impaired glucose metabolism contribute to the pathophysiology of AD.
These factors can lead to neuronal dysfunction and death, further exacerbating the disease process.
Overall, the pathophysiology of AD is a complex interplay of multiple factors that ultimately lead to the progressive decline in cognitive function and memory loss that characterizes the disease.
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